Traumatic Brain Injury (TBI)

The treatment of TBI is critical; it is estimated that between 3.2 and 5.3 million Americans live with permanent disabilities as a direct result of a TBI(1). Traumatic brain injuries (TBI) refer to injuries to the brain caused by an external physical force(2). Such injuries result in brain dysfunction, which can lead to cognitive impairments such as decreased attention, memory loss, and reduced cognitive flexibility as well as motor issues(3). However, there is compelling evidence to suggest that HBOT may significantly reduce the negative symptoms experienced by TBI patients, even years after the incident.

 

Extivita Therapies for TBI:

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Extivita Therapies Traumatic Brain Injury Recovery:

Hyperbaric Oxygen Therapy

Hyperbaric Oxygen Therapy

Hyperbaric Oxygen Therapy

Neurofeedback

Hyperbaric Oxygen Therapy

Supplements

Hyperbaric Oxygen Therapy

Nutritional IV Therapy

Pulsed Electromagnetic Field Therapy (PEMF)

Pulsed Electromagnetic Field Therapy

Hyperbaric Oxygen Therapy for Traumatic Brain Injury:

HBOT has been shown to improve cognitive function and quality of life in patients who experienced a mild TBI(4). Additionally, HBOT results in improved cognitive function (in multiple categories) in the case of moderate and severe TBI as well. These improvements were correlated with increased activity in the brain regions associated with each cognitive impairment(4).
 
Research suggests that increased tissue oxygenation, improved cellular metabolism and mitochondrial function, and improved inflammatory response, to name a few, are responsible for improving the following cognitive impairments(5):
 

  • Improved Memory (most improvement)
  • Reduced Attention Problems (high improvement)
  • Improved Executive Function
  • Increased Information Processing Speed
  • Improved Motor Skills
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Effects of HBOT on Traumatic Brain Injury:

Decreases Inflammation

Decreased Inflammation

Hyperbaric oxygen therapy reduces systemic inflammation by increasing anti-inflammatory gene expression and decreasing proinflammatory genes.
Increases Stem Cell Production

Increased Stem Cell Activity

Hyperbaric oxygen therapy mobilizes stem progenitor cells (SPCs) from the bone marrow, creating the opportunity for tissue regeneration.
Grows New Blood Vessels

New Blood Vessel Formation

Hyperbaric oxygen therapy stimulates the formation of new blood vessels, healing injured tissues that were unable to get nutrients and oxygen.

Neurofeedback for Traumatic Brain Injury:

Neurofeedback has been shown to improve many of the cognitive issues that patients with traumatic brain injuries (TBIs) experience post-injury(6, 7). After a TBI, the brain must form new neural pathways to account for any brain tissue damaged by the TBI. These new connections play a vital role in restoring healthy brain function, and neurofeedback has been shown to help establish and help strengthen such connections(6). Most studies that use neurofeedback to help TBIs train to increase theta and alpha brainwaves in the occipital lobe (towards the back of the head). This has been shown to improve reduce stress (which has a negative physiological and emotional effect in TBIs), increase relaxation, and improve cognitive measures such as memory and processing speed. (6, 7, 8, 9).

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IV Therapy for Traumatic Brain Injury:

The combination of the Myer’s cocktail and glutathione IV’s can improve cognitive and motor function following traumatic brain injury. A principal issue post-TBI is the degree neuroinflammation, which is directly correlated to the severity of the short-term and long-term consequences of TBI. In TBI patients, the mitochondria in brain cells become damaged, activating immune cells (glia, microglia, and astrocytes). These immune cells release inflammatory cytokines which recruit even more inflammatory cells to the area. This results in brain cell swelling, death, decreased energy production, all of which lead to impaired cognitive and motor function(10).

The Myers cocktail IV contains Vitamin C and other antioxidants which have been shown to decrease oxidative stress and inflammatory responses. By doing do, the Myer’s cocktail can help minimize further cells damage and improve brain health and function after a TBI(11, 12). Glutathione, the master antioxidant, has been used to reduce oxidative stress and enhance cellular detoxification and can be part of a multi-modal therapy in correcting the metabolic crisis in TBI.

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Hyperbaric Oxygen Therapy - Chapel Hill
Hyperbaric Oxygen Therapy - Chapel Hill

Pulsed Electromagnetic Field Therapy for Traumatic Brain Injury:

Micro vessels play a significant role in overall course of vascular diseases. Dysfunction to this system has been linked to a multitude of illnesses. The PEMF device has been shown to optimize the microcirculatory system, increasing perfusion to tissues and organs. When used in conjunction with HBOT, oxygen rich blood can be delivered to these areas, where healing can begin (13).

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News & Research for for Traumatic Brain Injury:

Linear analysis of heart rate variability in post-concussive syndrome.

Aug 3, 2017 | ,

Heart rate variability (HRV) represents measurable output of coordinated structural and functional systems within the body and brain. Both mild traumatic brain injury (mTBI) and HRV are modulated by changes in autonomic nervous system function. We present baseline HRV results from an ongoing mTBI clinical trial. HRV was assessed via 24-hour ambulatory electrocardiography; recordings were segmented by physiological state (sleep, wakefulness, exercise, standing still). Time, frequency, and spatial domain measures were summarized and compared with symptoms, sleep quality, and neurological examination. Median low frequency/high frequency (LF/HF) ratio exceeded 1.0 across segments, indicating prevalence of sympathetic modulation. Abnormal Sharpened Romberg Test was associated with 29% LF/HF decrease (95% CI [2.1, 47.7], p=0.04); pathological nystagmus associated with decreased standard deviation of electrocardiogram R-R interval (SDNN) index (25% decrease, 95% CI [0.8, 43.4], p=0.04). Increased sympathetic modulation was associated with increased anger scores (19% LF/HF increase with 5-point State Trait Anger Expression Inventory-2 trait anger increase (95% CI [1.2, 39.1], p=0.04)). A 13% HF increase (95% CI [2.1, 25.7], p=0.02) was observed with increased Pittsburgh Sleep Quality Index scores. These results support autonomic nervous system dysfunction in service members after mTBI.

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Sleep assessments for a mild traumatic brain injury trial in a military population.

Aug 3, 2017 | ,

Baseline sleep characteristics were explored for 71 U.S. military service members with mild traumatic brain injury (mTBI) enrolled in a post-concussive syndrome clinical trial. The Pittsburgh Sleep Quality Index (PSQI), sleep diary, several disorder-specific questionnaires, actigraphy and polysomnographic nap were collected. Almost all (97%) reported ongoing sleep problems. The mean global PSQI score was 13.5 (SD=3.8) and 87% met insomnia criteria. Sleep maintenance efficiency was 79.1% for PSQI, 82.7% for sleep diary and 90.5% for actigraphy; total sleep time was 288, 302 and 400 minutes, respectively. There was no correlation between actigraphy and subjective questionnaires. Overall, 70% met hypersomnia conditions, 70% were at high risk for obstructive sleep apnea (OSA), 32% were symptomatic for restless legs syndrome, and 6% reported cataplexy. Nearly half (44%) reported coexisting insomnia, hypersomnia and high OSA risk. Participants with post-traumatic stress disorder (PTSD) had higher PSQI scores and increased OSA risk. Older participants and those with higher aggression, anxiety or depression also had increased OSA risk. The results confirm poor sleep quality in mTBI with insomnia, hypersomnia, and OSA risk higher than previously reported, and imply sleep disorders in mTBI may be underdiagnosed or exacerbated by comorbid PTSD.

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References
  1. Tbi_report_to_congress_epi_and_rehab-a.Pdf.” Accessed June 2, 2019. https://www.cdc.gov/traumaticbraininjury/pdf/tbi_report_to_congress_epi_and_rehab-a.pdf.
  2. Silver, J.M., T.W. McAllister, and D.B. Arciniegas. Textbook of Traumatic Brain Injury. American Psychiatric Publishing, 2018. https://books.google.com/books?id=ViKMDwAAQBAJ.
  3. Hadanny A, Abbott S, Suzin G, et al. Effect of hyperbaric oxygen therapy on chronic neurocognitive deficits of post-traumatic brain injury patients: retrospective analysis. BMJ Open 2018;8:e023387. doi: 10.1136/bmjopen-2018-023387 https://bmjopen.bmj.com/content/bmjopen/8/9/e023387.full.pdf
  4. Boussi-Gross R, Golan H, Fishlev G, et al. Hyperbaric oxygen therapy can improve post concussion syndrome years after mild traumatic brain injury – randomized prospective trial. PLoS One 2013;8(11):e79995 https://www.ncbi.nlm.nih.gov/pubmed/24260334
  5. Efrati S, Ben-Jacob E. Reflections on the neurotherapeutic effects of hyperbaric oxygen. Expert Rev Neurother 2014;14:233–6. https://www.tandfonline.com/doi/full/10.1586/14737175.2014.884928
  6. Munivenkatappa, Ashok, et al. “EEG Neurofeedback Therapy: Can It Attenuate Brain Changes in TBI?” NeuroRehabilitation, vol. 35, no. 3, IOS Press, Jan. 2014, pp. 481–84. content.iospress.com, doi:10.3233/NRE-141140.
  7. Bennett, Cathlyn N., et al. “Clinical and Biochemical Outcomes Following EEG Neurofeedback Training in Traumatic Brain Injury in the Context of Spontaneous Recovery:” Clinical EEG and Neuroscience, SAGE PublicationsSage CA: Los Angeles, CA, Dec. 2017. Sage CA: Los Angeles, CA, journals.sagepub.com, doi:10.1177/1550059417744899.
  8. Reddy, Rajakumari Pampa, et al. “Silent Epidemic: The Effects of Neurofeedback on Quality-of-Life.” Indian Journal of Psychological Medicine, vol. 36, no. 1, 2014, pp. 40–44. PubMed Central, doi:10.4103/0253-7176.127246.
  9. Reddy, Rajakumari P., et al. “Neurofeedback Training to Enhance Learning and Memory in Patient with Traumatic Brain Injury: A Single Case Study.” The Indian Journal of Neurotrauma, vol. 6, no. 1, June 2009, pp. 87–90. ScienceDirect, doi:10.1016/S0973-0508(09)80037-3.
  10. Cheng, G., Kong, R.‐h., Zhang, L.‐m. and Zhang, J.‐n. (2012), Mitochondria in traumatic brain injury and mitochondrial‐targeted multipotential therapeutic strategies. British Journal of Pharmacology, 167: 699-719. doi:10.1111/j.1476-5381.2012.02025.x
  11. KC, Sagan et al. “Vitamin C enters mitochondria via facilitative glucose transporter 1 (Glut1) and confers mitochondrial protection against oxidative injury.” FASEB journal : official publication of the Federation of American Societies for Experimental Biology vol. 19,12 (2005): 1657-67. doi:10.1096/fj.05-4107com
  12. Zhang, Xiao-Ying et al. “Vitamin C alleviates LPS-induced cognitive impairment in mice by suppressing neuroinflammation and oxidative stress.” International immunopharmacology vol. 65 (2018): 438-447. doi:10.1016/j.intimp.2018.10.020
  13. https://www.imin-org.eu/images/science/Haug-Report-Bemer_2016_Englisch.pdf